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Biology of Disease > Infectious Agents (Prions, Fungi, Parasites) > Flashcards

Infectious Agents (Prions, Fungi, Parasites) Flashcards

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1
Q

What class of diseases do prions cause? Give examples.

A

Transmissible spongiform encephalopathies (TSEs)

Such as Creutzfeldt-jacob or Fatal familial insomnia or mad cow disease.

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2
Q

How can prions be detected?

A

Native proteins so no adaptive immune response.

Protease bio-assay:
- PrP samples degraded by proteases but PrPsc is resistant hence shows prion

Antibodies:
- No natural antibodies but can be manufactured

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3
Q

Compare the difference in structures of the native and prion PrP protein.

A

Normal:
- Alpha helical
- GPI anchored on cell surface
- Highly conserved (especially in CNS)

Infectious:
- Mainly beta sheets (huge conformational change)
- Very stable and resists protease degradation
- Catalyses conversion to PrPsc (+ve feedback)

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4
Q

How does PrPsc cause its pathology?

A
  • PrPsc accumulates forming oligomers and stable amyloid plaques
  • Either by spontaneous conversion or induced
  • Results in cell death and spongiform encephalopathies
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5
Q

Detail the transmission mechanisms of prions:

A

Sporadic:
- Cannibalism (e.g. kuru)
- Eating infected animals (scrapie, vCJD, BSE)
E.g. BSE epidemic due to infected bone meal fed to cattle and led to culling of 4.4m cattle

Familial:
- Can be used favourably for scrapie resistant sheep

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6
Q

Describe the structure of fungal cell wall.

A
  • Outer layer: mainly glucan (glucose β-1,3 linked polymer) and mannan (mannose polymer)
  • Inner layer: chitin microfibrils (β-1,4 linked residues)
  • Embedded glycoproteins: asparagine N-linked mannose/galactose residues or O-linked mannose/galactose
  • Outer polysaccharide capsule (optional) – determinant for virulence
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7
Q

What are the broad groups of fungi? (3 types)

A

Yeasts:
- Unicellular and replicate by mitosis (symmetrical binary fission/asymmetrical budding)

Filamentous moulds:
- Hypha, cells can be partitioned by septa
- Hyphae exhibit apical growth (longitudinal extension) and can form a mass = mycelium
E.g. Aspergillus

Dimorphic fungi:
- Can have different morphologies under different environmental conditions
- E.g. histoplasma is filamentous at 22°C but a yeast at 37°C

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8
Q

How do fungi reproduce?

A

Continue life cycle in either haploid or diploid state.

Asexual reproduction:
- Anamorph (mitotic state).
- Either produce external spores (conidium) on the outside of hyphae (aspergillus) or produce internal spores inside sporangium (specially adapted hypha)

Sexual reproduction:
- Teleomorph (meiotic state) Spores produced by fusion of two gametes.
- Allows chromosome reassortment and recombination

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9
Q

How can fungi cause disease?

A

Ingestion of a toxin (e.g. α-amanitin – binds strongly to RNA pol)

Inhalation of spores (causing hypersensitivity/asthma)

Skin contact when epithelium broken

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10
Q

How does the body protect against fungal disease?

A
  • Structural barriers e.g. skin
  • Commensal bacteria (provide competition to inhibit fungal multiplication)
  • PRR recognition and immune response (e.g. production of cytokines)
  • Activation of complement (MBLSP)
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11
Q

Give examples of PRRs against fungal infection:

A

Often mannose rich structures since uncommon in host.

  • General: IFN- γ and TNF-α (macrophage stimulation), IL-22 (neutrophil stimulation)

Specific PRRs:
- TLR-2 phospholipomannan
- TLR-4: O-linked mannose
- Dectin-2: mannan
- NLRP3 leads to pyroptosis

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12
Q

How can a fungal infection be identified? How can it be treated (broad classes)?

A
  • Grow in vitro from a sample (slow but can be drug tested)
  • Detection of a fungal polysaccharide/DNA
  • Tissue biopsy for microscopy

Treated by targeting:
- Membranes and polyenes
- Microtubules
- Cell walls (e.g. use caspofungin)

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13
Q

How does histoplasma infect and cause disease?

A

A temperature sensitive dimorphic yeast.

  1. Inhaled as spores (<24C)
  2. Warmed inside body and germinate into budding yeast (<37C) due to switch in gene expression
  3. Infect macrophages by expressing hsp60 receptor which is complementary to CD11 on macrophages
  4. Survive in macrophage vacuoles by secreting protease resistant calcium binding protein (CBP)
  5. May lead to granuloma formation
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14
Q

Give examples of pathogenic fungal species and their disease course.

A

Candida Albicans: through skin due to a defect. Secretes candidalysin toxin which damages epithelial cells.

Aspergillus: filamentous mould inhaled - can cause lung colonisation (particularly due to existing damage)

Cryptococcus neoformans: yeast in bird faeces. Inhaled then can colonise CNS leading to meningoencephalitis

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15
Q

Describe the different categories of parasites:

A

Protozoan: (trypanosomes; leishmania)
- Amoeboid
- Flagellar
- Ciliary
- Gliding motility (actin-myosin motor)

Apicomplexans (all protozoan): plasmodium; toxoplasma
- Micronemes use gliding motility

Metazoan: helminths
- Roundworms
- Flatworms: either cestodes (tapeworms) ot trematodes (e.g. schistosoma)

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16
Q

What structures and chemicals do apicomplexans have to aid their invasion of host cells?

A
  • Apoplast: used for lipid/fatty acid metabolism
  • Apical complex: groups of secretory organelles
  • Conoid structure on head helps invade forming a parasitophorous vacuole (protects from acidification)
  • Rhoptry secretions form PV
  • Dense granules help mediate host defences
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17
Q

What broad factors affect parasite disease severity?

A

Stage of lifecycle infected with:
- Grown tapeworm causes little damage but infection with eggs (wrong host) is very dangerous

Size

Tropism (type of cell and host infected)

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18
Q

How do single celled and helminths differ in their fight against the host?

A

Single celled often use immune evasion:
- Antigenic variation (trypanosomes have dense variant surface glycoprotein coat protecting from recognition)
- Hiding (plasmodium infect RBCs without MHC I)

Helminths more likely to use modulation:
- Dampen pro-inflammatory response (modulating of TGF-β decreasing M2 induction)
- Upregulation of natural modulators (e.g. Tregs)

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19
Q

Describe the life-cycle of toxoplasma:

A

Apicomplexan which cycles between cats and their prey.
1. Male and female gametocytes fuse in a cat’s intestine producing oocysts
2. Oocysts expelled in faeces and sporulate after several days (very hardy)
3. Spores ingested by rodent where oocyst dissolves in gut allowing penetration
4. Infect nucleated cells (macrophages) form a PV called a tachyzoite
5. Rapid proliferation through asexual reproduction, lysing and reinfection
6. Immune response clears most but some remain as bradyzoites (slow growing tissue cysts)
7. Cat eats rodent and becomes infected. Cycle continues.

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20
Q

Name the infection stages of toxoplasma, plasmodium, leishmania and schistosoma:
(using nomenclature)

A

Toxo:
- Tachyzoite (forms after initial rodent infection; fast growing)
- Bradyzoite (later form; slow growing)

Plasmodium:
- Sporozoite (in mosquito – infects human)
- Liver schizonts (develop after infection)
- Merozoites (infect RBCs)

Leishmania:
- Promastigotes in sandflies (procyclic initially then metacyclic)
- Amastigotes (when flagella are lost in phagolysosome)

Schisto:
- Cercariae in water
- larval schistosomula develop
- Miracidia hatch in water and invade snails.

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21
Q

What pathologies are associated with Toxoplasmosis? (In a mouse and human)

A

Humans:
- If healthy: mild symptoms due to inflammatory response
- If immunocompromised: can cause encephalitis or death
- If pregnant: can cross placental barrier causing congenital blindness or abortion.

Rats:
- Some evidence for increasing their courage (lose aversion to cat urine)

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22
Q

What are the 5 species of Plasmodium and any defining histology features:

A
  • Falciparum: RBCs slightly distorted but not enlarged; stippling (due to Maurer’s clefts)
  • Knowlesi: RBCs not distorted or enlarged (no stippling)
  • Malariae: Same as knowlesi but not all cells
  • Ovale: RBCs fibriated, enlarged and distorted. Fine stippling (Schaffner’s dots)
  • Vivax: RBCs enlarged and distorted. Darker patches from amoeboid trophozoites.
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23
Q

Describe the plasmodium life cycle:

A
  1. Female mosquito infected during a blood meal
  2. Plasmodium sexually reproduces forming sporozoites
  3. Sporozoites injected into vertebrate host where they infect hepatocytes
  4. Liver schizonts develop over 2 weeks (asymptomatic)
  5. Thousands of merozoites burst out and infect RBCs
  6. Cycle repeats when mosquito takes new meal
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24
Q

Why does Plasmodium cause cyclical symptoms?

A
  • Bursting of RBCs activates pro-inflammatory factors (IL-12, TNF-α, NO)
  • Cycle time of bursting and reinfection (time depends on species e.g. falciparum 48hrs; malariae 72hrs)
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25
Q

What immune evasion strategies does Plasmodium employ?

A
  • Tropism: infects RBCs with no MHC I
  • Antigenic variation: exports PfEMP1 onto surface with variable subunit (60 variable genes, all susceptible to somatic recombination as subtelomere)

Sequestering:
- PfEMP1 adapted to bind endothelial ICAMs – reduces spleen clearance of infected cells.
- Pro-inflammatory response upregulates ICAMs!
- Can bind RBCs together forming rosettes which are less mobile

26
Q

What are some natural resistances to Plasmodium?

A

Sickle cell trait: reduces invasion by falciparum and growth as sickle cells leak nutrients (particularly in low oxygen sites where infected cells normally sequester)

Thalassemia: smaller haemoglobin concentrations in more cells. Enhances parasite removal (thalassemia β) and reduced sequestering (thalassemia α).

G6PD deficiency: creates hostile environment to parasite by increasing oxidative stress.

27
Q

Describe the lifecycle of leishmania:

A

Entirely indirect (asexual reproduction)

  1. Infective metacyclic promastigotes infect a vertebrate via a sandfly bite
  2. Taken up by macrophages into a phagolysosome (low pH) and lose their flagellum (become amastigotes)
  3. Replicate and lyse cells
  4. Sandfly take up amastigotes during a blood meal
  5. Amastigotes turn back into procyclic promastigotes which then asexually reproduce into mature metacyclic promastigotes.
28
Q

How do leishmania surface antigens aid their infection?

A

Lipophosphoglycan (LPG) is a surface antigen:

  • Protects Leishmania in sandfly gut and reduces risk of defecation by anchoring
  • Protects from complement attack and oxidative bursts
  • Can change and become more decorated in mammal
29
Q

What disease can leishmania cause?

A
  • Cutaneous (ulcers)
  • Diffuse cutaneous
  • Mucocutaneous: destroys mucosal layers in nose and can metastasise
  • Visceral disease
30
Q

What is the ‘unholy triad’ and why is it dangerous?

A

Infection with 3 nematodes: hookworm, whipworm and giant roundworm.

  • Worst affect in children and women due to anaemia tendency.
31
Q

Describe the lifecycle and pathology of hookworm:

A

Lifecycle: indirect
- Eggs hatch in soil into larvae which penetrate the skin
- Move in bloodstream into lungs; get coughed up and swallowed into GI tract
- Find mate in tract and produce eggs

Pathology:
- Worms feed causing anaemia and malnutrition
- Secrete anticoagulant causing bleeding
- Distended belly and reduced growth (canine hookworm can cause skin eruptions)

32
Q

Describe the lifecycle and pathology of whipworm (Trichuris)

A

Life cycle: faecal-oral

  • Eggs ingested and develop into adults (3 months later)
  • Thin end threads into mucosal lining of intestinal wall to feed and produce eggs

Pathology:
- No bleeding involved but infection often leads to anaemia – due to pore-forming toxin causing generalised bone marrow failure
- Malabsorption, diarrhoea and rectal swelling

33
Q

Describe some differences in tropism between Plasmodium species:

A

Age of RBCs infected:
- Vivax/ovale = young
- Malariae/Knowlesi = old
- Falciparum = all

Antigens:
- Vivax binds to duffy antigen on RBCs (absent on sickle cells)

34
Q

Describe the lifecycle and pathology of Roundworm:

A

Lifecycle: same as hookworm but do not attach to intestine, instead feed in lumen

Pathology: severity depends on size of worm burden
- Allergic reactions, blockages and malnutrition
- Anti-trypsin factor released interfering with absorption

35
Q

Describe the lifecycle and pathology of pinworm:

A

Lifecycle: faecal oral transmission
- Worms reach rectum and crawl to peri-anal region to lay eggs at night
- Eggs spread by scratching and become infectious within hours (very fast!)

Pathology:
- Very little
- Skin irritation

36
Q

Describe the lifecycle of tapeworms:

A

Lifecycle: usually require two hosts (definitive and intermediate)
- Larvae form cysts in animal tissue after ingestion
- Humans ingest larvae which develop into segmented adults (up to 10m long)
- Each segment (proglottid) is either male or female and will detach when mature – containing up to 50,000 eggs!

37
Q

Describe the pathology of tapeworms:

A

Infection is generally asymptomatic
- Several diseases caused by ingestion of eggs into an intended definitive host e.g cysticercosis (huge cysts form and cause pressure)
- If cysts form in the brain seizures can result.

38
Q

Describe the lifecycle of Schistosoma:

A
  • Cercariae in water penetrate the skin
  • Larval schistosomula develop into worms
  • Adult female and male pair (spooning)
  • Attach to mesenteric venules in liver or venous plexus around bladder.
  • > 300 eggs deposited daily moving into intestines
  • Once in water they hatch forming miracidia which invades snails
39
Q

Describe the pathology and immune response to Schistosoma:

A

Pathology:
- Intestinal/bladder disease
- Hepatosplenomegaly or calcification of the liver
- Bladder fibrosis or “sandy patches” on the cervix

Stray eggs cause more pathology due to:
- Granulomas
- Blocked blood vessels

Immune response:
- Initial Th1 response due to cercariae penetration
- Egg deposition switches response to Th2. Modifies later by Treg and IL-10

40
Q

What are the different levels of parasite control?

A

Eradication: ideal but unlikely (due to vector hosts)

Elimination = eradication in a particular geographical location (e.g. schistosomiasis in Japan)

Control: effective for diarrhoeal diseases

41
Q

Describe an example of parasitic elimination:

A

Schistosomiasis. Japonica eliminated in Japan through:
- Infrastructure: reduced snail breeding in rice fields
- Drugs: killed snails; human treatments
- Reservoir reduction: replaced cows with horses (who do not carry parasite)

42
Q

Why has leishmania been hard to control in India?

A
  • Sandfly population large and resistance beginning to insecticide
  • Leishmania diagnosis hard (requires blood test and therefore infrastructure)
  • Treatment unpleasant and toxic.
43
Q

Why have vaccines not been effective against parasites?

A
  • High antigenic diversity
  • Many different developmental stages (with different appearances)
  • Host control and immune evasion
44
Q

How is Malaria being targeted for vaccine given difficulty of vaccine development?

A

Targets lifecycle at population bottleneck:
- Sporozoites and gametocytes since many fewer parasites.
- Want to target liver stage to prevent progression to blood stage

RTS,S vaccine promising
- Consists of virus like particle and hepatitis B surface antigen (S)

45
Q

How can transmission of parasites be targeted? (give examples)

A

Target mosquitos and sandfly populations:

  • Wolbachia introduction associated with lower parasitic burden in mosquitoes
  • DDT targeting mosquitos in sub-Saharan Africa. Effective but ecological problems.

Physical barriers:
- Pyrethroid-impregnated bed nets.

Gene drive:
- Genetic engineering to encourage expression of gene above Mendelian rate. - Can be sex skewed or fertility reducing.

46
Q

Describe some effective chemotherapies against parasites:

A

Preventative drugs:
- Albendazole: used for intestinal parasites as annual deworming programme (effective in schools of low income countries)
- Ivermectin for worms in cattle; scabies in pigs…

Therapeutic treatments (after infection):
- Praziquantel for schisto
- Artemisinin combination therapy (ACT) for malaria

47
Q

What are filarial worms?

A

Thread like nematodes (roundworms)
- 8 species which colonies combination of lymphatics, subcutaneous and serous tissue.
- Transmitted through indirect lifecycle
- Exist as microfilariae and long lived adult worms

48
Q

Why are filarial worms hard to understand, study and treat?

A
  • Disease associated with dying worms (can interfere with treatment)
  • Cannot be grown in lab
  • Chronic infection common
49
Q

How do filarial worms modulate the immune system?

A
  • Modulate plasma cell response
  • Block certain classes of immune cells
  • Block B cells but allow Treg cells to proliferate
  • Induce apoptosis in targeted immune populations

Chemokine/cytokines:
- Mimic host
- Leukocyte modulators

50
Q

Describe the disease caused by W.Bancrofti:

A

Lymphedema of extremities:
- Testicular lymphedema
- Elephantiasis

Disease:
- Large range in effect (can be microfilariae +ve without disease
- Can have high IL-4 and low IFN-gamma but no pathology
- Dying worms cause pathology (chronic disease)
- High IFN-γ; IL-17 and IL-4

51
Q

How does W.Bancrofti modulate the immune system? What are the treatment options?

A

Immune modulation:
- Reduces lymph viscosity (keeps it flowing)
- Leukocyte production

Treatment:
- DEC kills microfilariae and blocks transmission but doesn’t kill adult worms
- No adult worm drug (to eliminate adult worms)
- Wolbachia important

52
Q

Describe the lifecycle of O.volvulus:

A

Life cycle specifics:
- Transmitted by blackfly
- Male and female worms live intertwined in nodules
- Produce microfilariae which migrate and cause inflammation

53
Q

What diseases does O.volvulus cause?

A

Pathology:
- River blindness (due to immune response from worms moving through eye
- Depends on where bitten (bitten closer to eye = higher chance)
- Severe dermatitis (Due to worms moving)

Spectrum of disease (People can be microfalimic without major symptoms)
- Immune people in endemic areas
- Chronic pathology (due to overactive Th2 immune response)

54
Q

What disease is caused by Loa Loa?

A

Subcutaneous filariasis:
- Circulating microfilaria elicit Calabar swelling and eosinophilia (IL-5)
- Fairly mild

Killing lots of worms can be deadly (when high parasitemia)
- Encephalitis

55
Q

How can O.volvulus be treated?

A
  • Ivermectin: effective but needs repeated administration and doesn’t kill adult worms
  • Treatment can depend on individual parasitemia to prevent reaction to dead worms.
56
Q

How can Loa Loa worm be treated? What are problems with this treatment?

A
  • Administration of DEC will kill both microfilaria and adults
  • Must be given repeatedly (worms long lived)

Problems with treatment:
- Killing lots of worms at once (when high parasitaemia) can cause severe disease e.g. encephalitis
- Treatment reaction dependent on individual.

57
Q

What are some problems with treating filaria in endemic areas with several species present:

A

Cross-reactivity:
- Ivermectin and Loa Loa can cause allergic encephalopathy
- DEC in O.volvulus results in Mazzotti allergic reaction

High parasitemia:
- Reactions can result from killing many worms at once

Killing worms in eye can cause opacity and blindness

58
Q

How can people be treated who are infected with several filarial worm species?

A

First:
Killing O.volvulus and W.Bancrofti by killing Wolbachia (using doxycycline):
- Flies need Wolbachia to reproduce
- Worms need Wolbachia to live

Second;
- kill any Loa Loa using DEC

59
Q

How does Ivermectin work?

A
  • Binds to glutamate gated Cl- channels
  • Causes paralysis in worm
  • Doesn’t affect humans as cannot cross BBB (where our complementary channels are)
60
Q

Describe the form and efficacy of newly developed malaria vaccines:

A
  • Virus like particle vaccine targeting the pre-erythrocytic stage
  • RTS.S vaccine displays P.Falciparum circumsporozoite RTS protein
  • Shows 51.3% efficacy in children
  • However, no effect on transmission

Biology of Disease (7 decks)

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